Many developmental disorders arise from abnormalities in neurotransmission, neuronal connectivity, and/or neuron/glia interactions. It is thus essential to elucidate the mechanisms underlying the establishment of neuronal networks, including cortical network, to propose new therapies or markers aiming at preventing the occurrence of such brain deficits in childs. Our group is focused on the function of Selenoprotein T during neurodevelopment, and its contribution to the regulation of redox homeostasis during the establishment of functional circuitry.

Our research unit has characterized Selenoprotein T as a Selenium-containing protein expressed in the central nervous system during development. Using genetic invalidation models in mice, we have demonstrated that this protein contributes to the control of redox homeostasis and neuroblast survival. These alterations detected in the knockout animals lead to behavioral deficits, which manifest in the absence of gross morphological abnormalities.

Murine models, supplemented with more specific approaches, such as in utero electroporation are being used to contribute deciphering the mechanisms underlying the complex origin of cognitive functions, and how they can be altered during pathophysiological conditions, such as ASD or ADHD.